Mechanisms of development and general features
The key clinical manifestation of paroxysmal tachycardia is the sudden onset of the attack and its equally sudden termination (the so-called "on-off phenomenon"). Unlike atrial fibrillation, where the pulse is chaotic, here the pulse wave remains regular.
The main pathological mechanism is re-entry—re-entrant excitation and its circulation through a closed loop. Much less commonly, the cause is an enhanced automaticity of myocardial cells. For formal ECG confirmation of the diagnosis, it is necessary to record a "run" of several consecutive extrasystoles (three or more for supraventricular and five or more for ventricular rhythms).
Supraventricular tachycardia
At high heart rates, the P wave on the electrocardiogram often merges with the QRS complexes, which is why atrial and atrioventricular forms are grouped together as supraventricular tachycardias.
- Atrial form. The origin is located in the atrial myocardium. It occurs predominantly in organic heart diseases (coronary artery disease, cor pulmonale) or in cardiac glycoside overdose. On the ECG, a deformed P wave may be registered before each QRS complex. Concomitant AV block is possible.
- Atrioventricular form. The re-entry mechanism is localized in the AV junction or in accessory pathways (WPW syndrome). Unlike the atrial form, it frequently occurs in young individuals without organic myocardial pathology. Pronounced autonomic symptoms are characteristic: fear, dizziness.
General ECG features: narrow (unchanged) QRS complex, P wave (if visible) inverted in leads II, III, aVF due to retrograde conduction. Vagal maneuvers (stimulation of the vagus nerve) are used for emergency termination of the attack: carotid sinus massage, Aschner sign (ocular pressure), Valsalva maneuver, or inducing a gag reflex.
Paroxysmal ventricular tachycardia (PVT)
This is an extremely dangerous condition originating in the ventricles or bundle of His branches. PVT is always associated with severe organic pathology (myocardial infarction, heart defects) or acute intoxication. The arrhythmia severely impairs hemodynamics, causes progressive ischemia, and often serves as a precursor to ventricular fibrillation.
ECG criteria for PVT:
- AV dissociation. Atria and ventricles contract independently. The ventricular rate is significantly faster than the atrial rate (P waves are not related to QRS complexes).
- Wide QRS. The complex is sharply deformed and widened (in 75% of cases, more than 0.14 seconds).
- Discordance. The ST segment and T wave are directed opposite to the main deflection of the QRS complex.
A specific variant is torsade de pointes. This is a spindle-shaped form in which the amplitude and morphology of the QRS complexes wax and wane in a wave-like manner.
Role of the Q-T interval
Episodes of ventricular tachycardia often manifest against the background of a prolonged Q-T interval, which carries a high risk of sudden cardiac death. Prolongation can be either congenital or acquired.
Causes of acquired Q-T prolongation:
- Electrolyte depletion (hypokalemia, hypomagnesemia, hypocalcemia).
- Endocrine and metabolic disorders (starvation, hypothyroidism, anorexia).
- Iatrogenesis (administration of antiarrhythmic or psychotropic drugs).
- Pronounced bradycardias (AV blocks, sick sinus syndrome).
Briefly: answers to topical questions
Which antiarrhythmic drugs are used for the pharmacological cardioversion of ventricular tachycardia?
For the pharmacological cardioversion of ventricular tachycardia, drugs from several classes are used depending on the clinical situation.
- Lidocaine is the drug of choice, demonstrating high efficacy in myocardial infarction.
- Moracizine (ethmozine) is also among the drugs of choice for this pathology.
- Amiodarone is administered intravenously in combination with beta-blockers (e.g., non-selective propranolol) in structural heart disease and electrical storm.
- Procainamide can be used as an alternative; its use depends on the etiology of the arrhythmia.
What is the technique for performing carotid sinus massage during an attack of tachycardia?
Technique for performing carotid sinus massage during an attack of tachycardia:
- Patient position — supine, preferably with elevated legs.
- Status monitoring — must be performed under obligatory pulse monitoring; continuous ECG and blood pressure monitoring are also described for carotid sinus massage.
- Method of application — sources on supraventricular tachycardia indicate performing carotid sinus massage on only one side; the guidelines on paroxysmal tachycardia also describe alternating right and left application.
- Duration of the vagal maneuver during tachycardia is 15–20 seconds.
- Before performing carotid sinus massage, the CSM technique source indicates ruling out contraindications: auscultation of the carotid arteries and duplex scanning of brachiocephalic arteries with color Doppler flow imaging.
To differentiate the type of tachycardia on an ECG, use the rule "Narrow on top, wide on the bottom." If the origin is "on top" (in the atria or AV node), the impulse travels via normal pathways, so the QRS complex remains narrow. If the focus is "on the bottom" (in the ventricles), the conduction pathways are altered, and the QRS is wide.
Class and exam questions
What is AV dissociation?
This is independent contraction of the atria and ventricles, with no fixed relationship between P waves and QRS complexes. It is a critical diagnostic sign of ventricular tachycardia.
Why is the P wave sometimes negative in the supraventricular form?
Due to retrograde conduction of the electrical impulse from the AV junction bottom-up to the atria.
What else to study on this topic
- Mechanism of re-entrant excitation wave circulation (re-entry) at the electrophysiological level.
- Wolff-Parkinson-White (WPW) syndrome and accessory pathways.
- Pathophysiology of polymorphic tachycardia (torsade de pointes).
- Differences between right and left ventricular forms of paroxysmal tachycardia.
- Digitalis intoxication: mechanisms of effect on rhythm and conduction.
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